PAR2

F2RL1
Identifiants
Aliases	F2RL1, PAR2, Protease-Activated Receptor-2, Coagulation factor II receptor-like 1
IDs externes	OMIM: 600933 MGI: 101910 HomoloGene: 21087 GeneCards: F2RL1
Position du gène (Homme)
Chr.	Chromosome 5 humain
Fin	76,835,315 bp
Position du gène (Souris)
Chr.	Chromosome 13 (souris)
Fin	95,661,735 bp
Expression génétique
	Fortement exprimé dans
	mucosa of sigmoid colon; ; muqueuse jéjunale; ; skin of thigh; ; duodénum; ; tubule rénal; ; rectum; ; skin of hip; ; gingival epithelium; ; mucosa of ileum; ; mucosa of transverse colon;
	Fortement exprimé dans
	epithelium of stomach; ; vestibular membrane of cochlear duct; ; left colon; ; glande pinéale; ; iléon; ; corneal stroma; ; mucous cell of stomach; ; antre du pylore; ; Jéjunum; ; lèvre;
	Plus de données d'expression de référence
	; ;
	Plus de données d'expression de référence
Gene Ontology
Fonction moléculaire	G protein-coupled receptor activity; signal transducer activity; thrombin-activated receptor activity; G-protein beta-subunit binding; liaison protéique; G-protein alpha-subunit binding; signaling receptor binding; signaling receptor activity;
Composant cellulaire	integral component of membrane; appareil de Golgi; pseudopode; membrane; membrane plasmique; integral component of plasma membrane; early endosome;
Processus biologique	positive regulation of Rho protein signal transduction; establishment of endothelial barrier; thrombin-activated receptor signaling pathway; neutrophil activation; positive regulation of phagocytosis, engulfment; positive regulation of toll-like receptor 3 signaling pathway; positive regulation of eosinophil degranulation; positive regulation of neutrophil mediated killing of gram-negative bacterium; negative regulation of tumor necrosis factor-mediated signaling pathway; processus du système immunitaire; positive regulation of cell migration; positive regulation of cytosolic calcium ion concentration; coagulation sanguine; positive regulation of JNK cascade; positive regulation of leukocyte chemotaxis; negative regulation of JNK cascade; leukocyte proliferation; regulation of JNK cascade; positive regulation of pseudopodium assembly; positive regulation of renin secretion into blood stream; defense response to virus; positive regulation of chemotaxis; positive regulation of ERK1 and ERK2 cascade; positive regulation of toll-like receptor 4 signaling pathway; positive regulation of I-kappaB kinase/NF-kappaB signaling; positive regulation of toll-like receptor 2 signaling pathway; positive regulation of phosphatidylinositol 3-kinase signaling; positive regulation of superoxide anion generation; positive regulation of glomerular filtration; regulation of blood coagulation; réponse inflammatoire; système immunitaire inné; mature conventional dendritic cell differentiation; negative regulation of toll-like receptor 3 signaling pathway; positive regulation of actin filament depolymerization; leukocyte migration; regulation of I-kappaB kinase/NF-kappaB signaling; positive regulation of transcription by RNA polymerase II; positive regulation of positive chemotaxis; transduction de signal; T cell activation involved in immune response; positive regulation of cytosolic calcium ion concentration involved in phospholipase C-activating G protein-coupled signaling pathway; G protein-coupled receptor signaling pathway; positive regulation of GTPase activity; cell-cell junction maintenance;
	Sources:Amigo / QuickGO
Orthologues
	2150
	14063
	ENSG00000164251
	ENSMUSG00000021678
	P55085
	P55086
	NM_005242
	NM_007974
	NP_005233
	NP_032000
	Wikidata
Voir/Editer Humain	Voir/Editer Souris

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Le PAR2 (« Protease-Activated Receptor-2 »), ou F2RL1 (« coagulation factor II receptor-like 1 ») est un récepteur (biochimie) cellulaire de la famille des récepteurs activés par la protéase et intervient dans les syndromes inflammatoires et dans certaines infections. Son gène est F2RL1 situé sur le chromosome 5 humain.

Rôle dans les infections

Ce récepteur peut être stimulé par le virus herpès simplex de type 1^[5]. Il intervient dans le contrôle des récepteurs de type Toll (TLR), inhibant le TLR3^[6] et interagissant avec le TLR4^[7].

Il aurait un rôle protecteur contre les infections par le virus de la grippe A^[8].

Son activation par le virus coxsackie B 3 jouerait un rôle dans la dysfonction cardiaque au cours d'une myocardite à ce virus^[9].

Son expression au niveau cardiaque est diminué en cas d'insuffisance cardiaque à fraction d'éjection préservée, avec une augmentation de la fibrose^[10].

Notes et références

↑ ^{a b et c} GRCh38: Ensembl release 89: ENSG00000164251 - Ensembl, May 2017
↑ ^{a b et c} GRCm38: Ensembl release 89: ENSMUSG00000021678 - Ensembl, May 2017
↑ « Publications PubMed pour l'Homme », sur National Center for Biotechnology Information, U.S. National Library of Medicine
↑ « Publications PubMed pour la Souris », sur National Center for Biotechnology Information, U.S. National Library of Medicine
↑ Sutherland MR, Ruf W, Pryzdial EL, Tissue factor and glycoprotein C on herpes simplex virus type 1 are protease-activated receptor 2 cofactors that enhance infection, Blood, 2012;119:3638–3645
↑ Nhu QM, Shirey K, Teijaro JR et al. Novel signaling interactions between proteinase-activated receptor 2 and Toll-like receptors in vitro and in vivo, Mucosal Immunol, 2010;3:29–39
↑ Rallabhandi P, Nhu QM, Toshchakov VY et al. Analysis of proteinase-activated receptor 2 and TLR4 signal transduction: a novel paradigm for receptor cooperativity, J Biol Chem, 2008;283:24314–24325
↑ Khoufache K, LeBouder F, Morello E et al. Protective role for protease-activated receptor-2 against influenza virus pathogenesis via an IFN-gamma-dependent pathway, J Immunol, 2009;182:7795–7802
↑ Weithauser A, Bobbert P, Antoniak S et al. Protease-Activated Receptor-2 regulates the innate immune response to viral infection in a Coxsackievirus B3–induced myocarditis, J Am Coll Cardiol, 2013;62:1737-1745.
↑ Friebel J, Weithauser A, Witkowski M et al. Protease-activated receptor 2 deficiency mediates cardiac fibrosis and diastolic dysfunction, Eur J Cardiol, 2019;40:3318–3332

[refGRCh38Ensembl-1] {a b et c} GRCh38: Ensembl release 89: ENSG00000164251 - Ensembl, May 2017

[refGRCm38Ensembl-2] {a b et c} GRCm38: Ensembl release 89: ENSMUSG00000021678 - Ensembl, May 2017

[3] « Publications PubMed pour l'Homme », sur National Center for Biotechnology Information, U.S. National Library of Medicine

[4] « Publications PubMed pour la Souris », sur National Center for Biotechnology Information, U.S. National Library of Medicine

[Sutherland_2012-5] Sutherland MR, Ruf W, Pryzdial EL, Tissue factor and glycoprotein C on herpes simplex virus type 1 are protease-activated receptor 2 cofactors that enhance infection, Blood, 2012;119:3638–3645

[Nhu_2010-6] Nhu QM, Shirey K, Teijaro JR et al. Novel signaling interactions between proteinase-activated receptor 2 and Toll-like receptors in vitro and in vivo, Mucosal Immunol, 2010;3:29–39

[Rallabhandi_2008-7] Rallabhandi P, Nhu QM, Toshchakov VY et al. Analysis of proteinase-activated receptor 2 and TLR4 signal transduction: a novel paradigm for receptor cooperativity, J Biol Chem, 2008;283:24314–24325

[Khoufache_2009-8] Khoufache K, LeBouder F, Morello E et al. Protective role for protease-activated receptor-2 against influenza virus pathogenesis via an IFN-gamma-dependent pathway, J Immunol, 2009;182:7795–7802

[Weithauser_2013-9] Weithauser A, Bobbert P, Antoniak S et al. Protease-Activated Receptor-2 regulates the innate immune response to viral infection in a Coxsackievirus B3–induced myocarditis, J Am Coll Cardiol, 2013;62:1737-1745.

[Friebel_2019-10] Friebel J, Weithauser A, Witkowski M et al. Protease-activated receptor 2 deficiency mediates cardiac fibrosis and diastolic dysfunction, Eur J Cardiol, 2019;40:3318–3332

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